A dysrhythmia is an abnormal heart beat pattern. One example of a dysrhythmia is a bradycardia wherein the heart beats at an abnormally slow rate or wherein significant pauses occur between consecutive beats. Other examples of dysrhythmias include tachyarrhythmias wherein the heart beats at an abnormally fast rate. With atrial tachycardia, the atria of the heart beat abnormally fast. With ventricular tachycardia (VT) the ventricles of the heart beat abnormally fast. Though often unpleasant for the patient, a tachycardia is typically not fatal. However, some tachycardias, particularly ventricular tachycardia, can trigger ventricular fibrillation wherein the heart beats chaotically such that there is little or no net flow of blood from the heart to the brain and other organs. Ventricular tachycardia, if not terminated, is fatal. Hence, it is highly desirable to prevent or terminate dysrhythmias, particularly ventricular tachycardias.
One technique for preventing or terminating dysrhythmias is to overdrive pace the heart wherein an implantable cardiac stimulation device, such as a pacemaker or implantable cardioverter defibrillator (ICD), applies electrical pacing pulses to the heart at a rate somewhat faster than the intrinsic heart rate of the patient. For bradycardia, the cardiac stimulation device may be programmed to artificially pace the heart at a rate of 60 to 80 pulses per minute (ppm) to thereby prevent the heart from beating too slow and to eliminate any long pauses between heart beats. To prevent tachyarrhythmias from occurring, the cardiac stimulation device artificially paces the heart at a rate of at least five to ten pulses per minute faster than the intrinsic tachyarrhythmia heart rate of the patient. In other words, a slight artificial tachycardia is induced and maintained in an effort to prevent an actual tachycardia from arising. If an actual tachycardia occurs, such as a supraventricular tachycardia (SVT) wherein the heart beats at 150 beats per minute or more, the cardiac stimulation device senses tachycardia and immediately begins pacing at a rate of at least five to ten pulses per minute (ppm) faster than the tachycardia and then slowly decreases the pacing rate in an effort to slowly reduce the heart rate back to a normal resting rate, thereby terminating the tachycardia.
Many patients who suffer from tachyarrhythmias have had episodes of ischemia wherein blood flow to the ventricular myocardium is reduced or blocked due to narrowing or occlusion of a coronary artery. This causes myocardial scarring, believed to present re-entrant circuits that can be triggered into sustained ventricular tachycardia or ventricular fibrillation by introduction of premature ventricular contractions (PVCs). A PVC is a ventricular contraction which is not preceded by a coupling atrial contraction (P wave). It is also at times assumed that a clinical episode of monomorphic ventricular tachycardia is also initiated by spontaneous PVCs. This assumption is reinforced by the known relationship between PVCs and sudden cardiac death. It would thus be beneficial if implantable cardiac devices could prevent PVCs from triggering ventricular tachyarrhythmias.
It is believed that dissociation between the left ventricle and the right ventricle may be responsible for PVCs. Further, it is believed that changes in the QRS complex on a surface electrocardiogram is the result of a dissociation in inter-chamber delay as, for example, the inter-ventricular delay (VR-VL Delay) or inter-atrial delay (AR-AL Delay). For example, the widening of the QRS complex (as is sometimes seen in monomorphic VT) may be the result of an increase in the VR-VL Delay. Furthermore, alternating amplitude of the QRS complex (as is sometimes seen in polymorphic VT) or P waves may be the result of a more significant dissociation in the VR-VL Delay or AR-AL Delay, respectively. It is further believed that if the VR-VL Delay becomes too great, then total dissociation between the left and right ventricles of the heart will result in a ventricular fibrillation and perhaps sudden cardiac death and that if the AR-AL Delay becomes too great, then total dissociation between the left and right atria of the heart will result in atrial fibrillation. It is still further believed that significant variability of inter-chamber delay, either of the ventricles or the atria, may also be prone to the development of ventricular fibrillation.